本文選題：高血壓 + 心血管重構(gòu)�。� 參考：《安徽醫(yī)科大學(xué)》2017年碩士論文

【摘要】：目的:探討心肌爾康多糖提取物對L-NAME誘導(dǎo)高血壓小鼠心血管重構(gòu)的影響,并對其可能的作用機制進(jìn)行了初步分析。方法:昆明種小鼠50只,♂,清潔級,按體重隨機分為對照組、模型組、多糖組、心肌爾康組和福辛普利組。除對照組外其余各組均以L-NAME誘導(dǎo)建立慢性高血壓模型,后三組在造模4weeks后再分別用心肌爾康多糖、心肌爾康全方以及陽性藥福辛普利繼續(xù)灌胃給藥4weeks,對照組小鼠8weeks內(nèi)均自由食水,每周末tail-cuff測定尾動脈收縮壓(systolic blood pressure,SBP),連續(xù)8weeks。第8周末,右頸動脈心臟插管測定各組小鼠左室舒張末期壓(left ventricular end-diastolic pressure,LVEDP)、左室收縮末期壓(left ventricular systolic pressure,LVSP)以及左心室壓力變化最大速率(maximal rate of left ventricular pressure,±dp/dtmax)。充分暴露胸腔取心臟、和主動脈胸段行相關(guān)指標(biāo)檢測。精密稱量小鼠體質(zhì)和心臟質(zhì)量并計算心重指數(shù)(心臟質(zhì)量/體質(zhì)量,HW/BW)。心臟切片經(jīng)蘇木素-伊紅(hematoxylin and eosin,HE)、膠原纖維(Van Gieson,VG)染色,胸主動脈經(jīng)蘇木素-伊紅(hematoxylin and eosin,HE)染色并分別觀察其病理學(xué)變化。內(nèi)皮依賴性血管舒張功能由體外血管環(huán)實驗測定。分別采用硫代巴比妥酸法(thiobarbituric acid,TBA)、黃嘌呤氧化酶法、硝酸還原酶法檢測血清中丙二醛(malondialdehyde,MDA)含量、超氧化物歧化酶(superoxide dismutase,SOD)活性、一氧化氮(nitric oxide,NO)的含量。酶聯(lián)免疫吸附測定(ELISA)法檢測血清中非對稱二甲基精氨酸(asymmetric dimethylarginine,ADMA)、內(nèi)皮型一氧化氮合酶(endothelial nitric oxide synthase,e NOS)的含量以及血清和心肌組織中白介素1β(interleukin 1β,IL-β)、腫瘤壞死因子α(tumor necrosis factorα,TNF-α)以及白介素10(interleukin 10、IL-10)的含量。采用免疫組化(immunocytochemistry)方法檢測心肌組織中IL-β、TNF-α、IL-10蛋白表達(dá)水平。結(jié)果:給藥4weeks后,與L-NAME模型組相比,心肌爾康多糖組,心肌爾康全方組,陽性藥福辛普利組明顯抑制SBP、HW/BW、LVSP和+dp/dtmax的升高(P0.01,P0.05)。病理學(xué)結(jié)果顯示,給予心肌爾康多糖,心肌爾康全方,陽性藥福辛普利處理4weeks后,心肌橫截面面積(cross-sectional area,CSA)、膠原容積分?jǐn)?shù)(collagen volume fraction,CVF)、血管周膠原面積(perivscular collagen area,PVCA)、中膜厚度(media thickness,MT)均明顯減小(P0.01),提高血清中SOD活性、e NOS活性(P0.01,P0.05),抑制血清中MDA含量、ADMA水平的升高(P0.01,P0.05)。心肌組織和血清中IL-β、TNF-α含量顯著降低(P0.01,P0.05)而IL-10含量明顯升高(P0.01,P0.05)。結(jié)論:心肌爾康多糖提取物通過改善內(nèi)皮功能紊亂、降低機體氧化應(yīng)激水平以及恢復(fù)免疫平衡,發(fā)揮對L-NAME誘導(dǎo)高血壓小鼠心血管重構(gòu)保護作用。
[Abstract]:Aim: to investigate the effect of Xinjinerkang polysaccharide extract on cardiovascular remodeling induced by L-NAME in hypertensive mice and its possible mechanism. Methods: fifty Kunming mice of clean grade were randomly divided into control group, model group, polysaccharide group, myocardial Erkang group and fosinopril group according to their body weight. The model of chronic hypertension was induced by L-NAME in all the other groups except the control group. The latter three groups were treated with Myocardial Erkang polysaccharide after 4weeks. Xin-er Kang Quan Fang and positive drug fosinopril continued to be administered intragastric for 4 weeks. Control mice were given free drinking water in 8weeks. Systolic blood pressure of the tail artery was measured by tail-cuff for 8 weeks at the end of the week. At the end of the 8th week, left ventricular end-diastolic pressure (LVEDP), left ventricular end-systolic pressure (LVSP) and maximal rate of left ventricular pressure change (maximal rate of left ventricular pressure, 鹵DP 路dtmax) were measured by right carotid artery catheterization. The heart and thoracic segment of aorta were detected. The body mass and heart mass of mice were accurately weighed and the heart weight index (heart mass / body mass) was calculated. The heart sections were stained with hematoxylin and eosin HEG, and the thoracic aorta were stained with hematoxylin and eosin HEG and the pathological changes were observed. Endothelium-dependent vasodilation function was measured by in vitro vascular ring experiment. The contents of malondialdehyde (malondialdehyde), superoxide dismutase (SOD) and nitric oxide (no) in serum were determined by thiobarbituric acid method, xanthine oxidase method and nitrate reductase method respectively. Enzyme-linked immunosorbent assay (Elisa) for the detection of asymmetric dimethylarginine (ADMA), endothelial nitric oxide synthase (Enos), interleukin 1 尾 (IL 1 尾), tumor necrosis factor 偽 (TNF- 偽) and endothelium nitric oxide synthase (Enos) in serum and myocardium The content of interleukin 10(interleukin 10 (IL 10). The expression of IL-10 protein in myocardial tissue was detected by immunocytochemistrymethod. Results: compared with the model group of L-NAME, the positive drug fosinopril inhibited the increase of SBPH-HW / BW-LVSP and dp/dtmax, compared with the model group of L-NAME, and the positive drug fosinopril inhibited the increase of SBPH-HW / BW-LVSP and dp/dtmax (P0.01) P0.05A, compared with the model group of L-NAME, the positive drug fosinopril group. The pathological results showed that after 4weeks was treated with Myocardial polysaccharides, Myocardial Kangquan recipe, positive drug fosinopril, Myocardial cross-sectional area, collagen volume fraction, perivascular collagen area, perivascular collagen area and media thickness significantly decreased P0.01G, increased the activity of SOD, P0.01P0.05, and inhibited the increase of MDA content in serum P0.01P0.05a. The content of IL- 尾 -TNF- 偽 in myocardium and serum decreased significantly (P 0.01), while the content of IL-10 increased significantly (P 0.01) and P 0.05 (P 0.05). Conclusion: the polysaccharides extract of Xinjinerkang can improve endothelial dysfunction, decrease the level of oxidative stress and restore the immune balance, so as to exert the protective effect on cardiovascular remodeling induced by L-NAME in hypertensive mice.
【學(xué)位授予單位】：安徽醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R965

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